Mechanism of allyl chloride-induced cytoskeletal injury to nerve cells.

To dissect the molecular mechanism of toxic neuropathy induced by allyl chloride (AC). Fluorescence molecular probe (Fura-2/AM), electron probe X-ray microprobe analysis (EPMA) and biochemical methods were used to determine the concentrations of cytosolic free Ca2+, the contents of intracellular Ca2+ percentage, Ca(2+)-free calmodulin (CaM), the activity of Ca2+/CaM-dependent protein kinase II (Ca2+/CaM-PK II), and cytoskeletal protein synthesis in chicken embryo brain cells induced by AC. The contents of Ca2+ percentage, the concentrations of cytosolic free Ca2+, and the activities of Ca2+/CaM-PK II in the cells were increased significantly as AC was added (P < 0.01). However, the content of Ca(2+)-free CaM and the synthesis of cytoskeletal proteins were markedly decreased (P < 0.01). The results suggest that one of the mechanism of AC-induced cytoskeletal injury in vitro might be related to the elevation of intracellular Ca2+, activated CaM and Ca2+/CaM-PK II.